Coronary artery spasm in intact dogs induced by potassium and serotonin

Although coronary artery spasm has been implicated as an important cause of myocardial ischemia in humans, an animal model of reversible segmental coronary constriction has not been described. To provoke coronary spasm in open-chest dogs, selected vasoconstricting agents adsorbed to viscous ion exchange gels were applied topically to the surface of epicardial coronary arteries. The procedure provided a sustained localized release of drug, and minimized effects on continguous myocardium or on the systemic circulation. Segmental arterial constrictor responses were evaluated by sonomicrometry, arteriography, and electromagnetic flow measurements. Potassium evoked sustained constrictions or spasms, and concomitantly reduced flow by -42 ± 4% (SE; n = 34). Serotonin likewise produced sustained decreases in flow of -22 ± 6% (SE; n = 5). Other contrictors, including norepinephrine and angiotensin, failed to evoke sustained constrictions. Spasms nearly abolished reactive hyperemic responses elicited by temporary complete occlusion of the artery. Intravenous nitroglycerin and dihydropyridine calcium antagonists promptly relieved the spasms. Scanning electronmicroscopic examination of the intimal surface of arteries undergoing sustained spasm revealed no platelet thrombi. Thus, nonthrombotic, vasodilator-sensitive segmental coronary spasms were elicited by endogenous constrictors which may play a role in regulating flow to ischemic myocardium.